Bailey.Glen at 21:24, 4 December 2023

2023-12-04T21:24:11Z

← Older revision		Revision as of 16:24, 4 December 2023
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	==Definition / Description of Disease==		==Definition / Description of Disease==

	MDS-RS-MLD is a subtype of [[Myelodysplastic Syndrome with Ring Sideroblasts (MDS-RS)\|MDS-RS]] which is features with the presence of ≥ 15% ring sideroblasts (RS) in erythroid precursor cells or ≥ 5% RS when ''SF3B1'' mutation is present. In prior version of WHO classification, it set refractory anaemia with ring sideroblasts (RARS) as one group and did not differentiate MDS-RS-SLD with MDS-RS-MLD. In 2016 WHO criteria, MDS-RS-MLD and MDS-RS-SLD were recognized as two separate subtypes of MDS-RS. Compared to MDS-RS-SLD that mainly affects erythroid lineage, MDS-RS-MLD usually has more than one cytopenia and more than two dysplasia in the three myeloid lineages such as erythroid, granulocytic and megakaryocytic lineages. According to 2016 WHO criteria, bone marrow (BM) blasts should be <5% and peripheral blood (PB) blast content should be <1%. In addition, MDS-RS is usually lack of Auer rods, and MDS with isolated del(5q) or RS with secondary causes must be excluded. Ring sideroblasts are erythroid precursor cells in which iron laden mitochondria form a perinuclear ring that can be visualized as blue granules by Prussian blue staining. RS can be found in other clonal neoplasms such as myelodysplastic/myeloproliferative neoplasm with ring sideroblasts and thrombocytosis ([[MDS/MPN-RS-T]]).		MDS-RS-MLD is a subtype of [[HAEM4:Myelodysplastic Syndrome with Ring Sideroblasts (MDS-RS)\|MDS-RS]] which is features with the presence of ≥ 15% ring sideroblasts (RS) in erythroid precursor cells or ≥ 5% RS when ''SF3B1'' mutation is present. In prior version of WHO classification, it set refractory anaemia with ring sideroblasts (RARS) as one group and did not differentiate MDS-RS-SLD with MDS-RS-MLD. In 2016 WHO criteria, MDS-RS-MLD and MDS-RS-SLD were recognized as two separate subtypes of MDS-RS. Compared to MDS-RS-SLD that mainly affects erythroid lineage, MDS-RS-MLD usually has more than one cytopenia and more than two dysplasia in the three myeloid lineages such as erythroid, granulocytic and megakaryocytic lineages. According to 2016 WHO criteria, bone marrow (BM) blasts should be <5% and peripheral blood (PB) blast content should be <1%. In addition, MDS-RS is usually lack of Auer rods, and MDS with isolated del(5q) or RS with secondary causes must be excluded. Ring sideroblasts are erythroid precursor cells in which iron laden mitochondria form a perinuclear ring that can be visualized as blue granules by Prussian blue staining. RS can be found in other clonal neoplasms such as myelodysplastic/myeloproliferative neoplasm with ring sideroblasts and thrombocytosis ([[MDS/MPN-RS-T]]).

	==Synonyms / Terminology==		==Synonyms / Terminology==

Bailey.Glen at 18:42, 3 November 2023

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← Older revision		Revision as of 13:42, 3 November 2023
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			{{DISPLAYTITLE:Myelodysplastic Syndrome with Ring Sideroblasts and Multilineage Dysplasia}}


			<blockquote class='blockedit'>{{Box-round\|title=PREVIOUS EDITION\|This page from the 4th edition of Haematolymphoid Tumours is being updated. See 5th edition [[HAEM5:Table_of_Contents\|Table of Contents]].
			}}</blockquote>
	==Primary Author(s)*==		==Primary Author(s)*==

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	==Notes==		==Notes==
	<nowiki>*</nowiki>Primary authors will typically be those that initially create and complete the content of a page. If a subsequent user modifies the content and feels the effort put forth is of high enough significance to warrant listing in the authorship section, please contact the CCGA coordinators (contact information provided on the homepage). Additional global feedback or concerns are also welcome.		<nowiki>*</nowiki>Primary authors will typically be those that initially create and complete the content of a page. If a subsequent user modifies the content and feels the effort put forth is of high enough significance to warrant listing in the authorship section, please contact the CCGA coordinators (contact information provided on the homepage). Additional global feedback or concerns are also welcome.
			[[Category:HAEM4]] [[Category:DISEASE]]

Bailey.Glen: Created page with " ==Primary Author(s)*== Xiaolin Hu, Ph.D., Teresa Smolarek, Ph.D, FACMG TOC ==Cancer Category/Type== Myelodysplastic Syndrome (MDS) ==Cancer Sub-Classification / Subt..."

2023-11-03T18:02:16Z

Created page with " ==Primary Author(s)*== Xiaolin Hu, Ph.D., Teresa Smolarek, Ph.D, FACMG __TOC__ ==Cancer Category/Type== Myelodysplastic Syndrome (MDS) ==Cancer Sub-Classification / Subt..."

New page

==Primary Author(s)*==

Xiaolin Hu, Ph.D., Teresa Smolarek, Ph.D, FACMG

__TOC__

==Cancer Category/Type==

Myelodysplastic Syndrome (MDS)

==Cancer Sub-Classification / Subtype==

MDS with Ring Sideroblasts and Multilineage Lineage Dysplasia (MDS-RS-MLD)

==Definition / Description of Disease==

MDS-RS-MLD is a subtype of [[Myelodysplastic Syndrome with Ring Sideroblasts (MDS-RS)|MDS-RS]] which is features with the presence of ≥ 15% ring sideroblasts (RS) in erythroid precursor cells or ≥ 5% RS when ''SF3B1'' mutation is present. In prior version of WHO classification, it set refractory anaemia with ring sideroblasts (RARS) as one group and did not differentiate MDS-RS-SLD with MDS-RS-MLD. In 2016 WHO criteria, MDS-RS-MLD and MDS-RS-SLD were recognized as two separate subtypes of MDS-RS. Compared to MDS-RS-SLD that mainly affects erythroid lineage, MDS-RS-MLD usually has more than one cytopenia and more than two dysplasia in the three myeloid lineages such as erythroid, granulocytic and megakaryocytic lineages. According to 2016 WHO criteria, bone marrow (BM) blasts should be <5% and peripheral blood (PB) blast content should be <1%. In addition, MDS-RS is usually lack of Auer rods, and MDS with isolated del(5q) or RS with secondary causes must be excluded. Ring sideroblasts are erythroid precursor cells in which iron laden mitochondria form a perinuclear ring that can be visualized as blue granules by Prussian blue staining. RS can be found in other clonal neoplasms such as myelodysplastic/myeloproliferative neoplasm with ring sideroblasts and thrombocytosis ([[MDS/MPN-RS-T]]).

==Synonyms / Terminology==

Refractory cytopenia with multilineage dysplasia and ring sideroblasts (RCMD-RS)

==Epidemiology / Prevalence==

*MDS-RS mainly affects elderly people with a median age of 60-73 years
*MDS-RS-MLD accounts for approximately 13% of all MDS cases
*No major sex predilection.

==Clinical Features==

*Usually present with bicytopenia or pancytopenia.
*Frequently has a higher IPSS-R score than MDS-RS-SLD.
*Symptoms with iron overload may be seen.

==Sites of Involvement==

*Primarily involves peripheral blood and bone marrow
*Liver and spleen may be affected by iron overload

==Morphologic Features==

Dyserythropoiesis is the most common dysplasia. In addition, significant dysplasia usually ≥ 10% can be seen in more than one non-erythroid lineages. Morphology of MDS-RS-MLD will be similar to those of MDS with multiple lineage dysplasia (MDS-MLD) except for the presence of ≥ 15% ring sideroblasts.

==Immunophenotype==

Currently, morphologic evaluation remains the gold standard in diagnosis of MDS. Immunophenotyping provides supportive evidence to clarify the blasts nature and percentage <ref>{{Cite journal|last=G|first=Zini|date=2017|title=Diagnostics and Prognostication of Myelodysplastic Syndromes|url=https://pubmed.ncbi.nlm.nih.gov/28840983/|language=en|doi=10.3343/alm.2017.37.6.465|pmc=PMC5587818|pmid=28840983}}</ref> . Flow cytometry may be used to characterize erythroid precursor cells. Della Porta M.G. et al proposed a set of immunophenotypic variables such as cytosolic H-ferritin, CD71 and CD105 to predict functionally aberrant erythropoietic precursors. They also reported mitochondrial ferritin (MtF) correlates well with the presence of ring sideroblasts and suggested MtF can be used in diagnosis of sideroblastic anemia <ref>{{Cite journal|last=Mg|first=Della Porta|last2=L|first2=Malcovati|last3=R|first3=Invernizzi|last4=E|first4=Travaglino|last5=C|first5=Pascutto|last6=M|first6=Maffioli|last7=A|first7=Gallì|last8=S|first8=Boggi|last9=D|first9=Pietra|date=2006|title=Flow Cytometry Evaluation of Erythroid Dysplasia in Patients With Myelodysplastic Syndrome|url=https://pubmed.ncbi.nlm.nih.gov/16498394/|language=en|pmid=16498394}}</ref>.

{| class="wikitable sortable"
|-
!Finding!!Marker
|-
|Positive (universal)||EXAMPLE CD1=
|-
|Positive (subset)||EXAMPLE CD2
|-
|Negative (universal)||EXAMPLE CD3
|-
|Negative (subset)||EXAMPLE CD4
|}

==Chromosomal Rearrangements (Gene Fusions)==

Put your text here and/or fill in the table

{| class="wikitable sortable"
|-
!Chromosomal Rearrangement!!Genes in Fusion (5’ or 3’ Segments)!!Pathogenic Derivative!!Prevalence
|-
|EXAMPLE t(9;22)(q34;q11.2)||EXAMPLE 3'ABL1 / 5'BCR||EXAMPLE der(22)||EXAMPLE 5%
|-
|EXAMPLE t(8;21)(q22;q22)||EXAMPLE 5'RUNX1 / 3'RUNXT1||EXAMPLE der(8)||EXAMPLE 5%
|}

==Characteristic Chromosomal Aberrations / Patterns==

Put your text here

==Genomic Gain/Loss/LOH==

About 50% of MDS-RS-MLD have cytogenetic abnormalities. High-risk abnormalities such as loss of chromosome 7 can be seen in this category.

{| class="wikitable sortable"
|-
!Chromosome Number!!Gain/Loss/Amp/LOH!!Region
|-
|EXAMPLE 8||EXAMPLE Gain||EXAMPLE chr8:0-1000000
|-
|EXAMPLE 7||EXAMPLE Loss||EXAMPLE chr7:0-1000000
|}

==Gene Mutations (SNV/INDEL)==

Somatic mutations in SF3B1 have been reported in several myeloid malignancies, especially MDS-RS. High occurrence rate of SF3B1 mutations has been observed in about 80% of patients with MDS-RS-SLD and 40% of patients with MDS-RS-MLD <ref>{{Cite journal|date=2015|title=Erratum: Borderud SP, Li Y, Burkhalter JE, Sheffer CE and Ostroff JS. Electronic Cigarette Use Among Patients With Cancer: Characteristics of Electronic Cigarette Users and Their Smoking Cessation Outcomes. Cancer. Doi: 10.1002/ cncr.28811|url=https://pubmed.ncbi.nlm.nih.gov/25855820/|language=en|pmid=25855820}}</ref><ref>{{Cite journal|last=E|first=Papaemmanuil|last2=M|first2=Cazzola|last3=J|first3=Boultwood|last4=L|first4=Malcovati|last5=P|first5=Vyas|last6=D|first6=Bowen|last7=A|first7=Pellagatti|last8=Js|first8=Wainscoat|last9=E|first9=Hellstrom-Lindberg|date=2011|title=Somatic SF3B1 Mutation in Myelodysplasia With Ring Sideroblasts|url=https://pubmed.ncbi.nlm.nih.gov/21995386/|language=en|doi=10.1056/NEJMoa1103283|pmc=PMC3322589|pmid=21995386}}</ref> . Most genetic alterations in SF3B1 are heterozygous missense variants that tend to cluster in C-terminal HEAT domains (residues 622–781). K700E accounts for 50% of these variants. Additional hotspots residues include 622, 625, 662 and 666. SF3B1 mutation is highly correlate with the presence of BM RS, and therefore was incorporated into 2018 WHO classification of MDS as a diagnostic criteria for MDS-RS when BM RS is over 5% or more. However, SF3B1 mutation alone does not confer diagnosis of MDS-RS. Several studies have demonstrated SF3B1 has a favorable prognostic impact <ref>{{Cite journal|last=N|first=Gangat|last2=M|first2=Mudireddy|last3=Tl|first3=Lasho|last4=Cm|first4=Finke|last5=M|first5=Nicolosi|last6=N|first6=Szuber|last7=Mm|first7=Patnaik|last8=A|first8=Pardanani|last9=Ca|first9=Hanson|date=2018|title=Mutations and Prognosis in Myelodysplastic Syndromes: Karyotype-Adjusted Analysis of Targeted Sequencing in 300 Consecutive Cases and Development of a Genetic Risk Model|url=https://pubmed.ncbi.nlm.nih.gov/29417633/|language=en|pmid=29417633}}</ref><ref>{{Cite journal|last=E|first=Papaemmanuil|last2=M|first2=Cazzola|last3=J|first3=Boultwood|last4=L|first4=Malcovati|last5=P|first5=Vyas|last6=D|first6=Bowen|last7=A|first7=Pellagatti|last8=Js|first8=Wainscoat|last9=E|first9=Hellstrom-Lindberg|date=2011|title=Somatic SF3B1 Mutation in Myelodysplasia With Ring Sideroblasts|url=https://pubmed.ncbi.nlm.nih.gov/21995386/|language=en|doi=10.1056/NEJMoa1103283|pmc=PMC3322589|pmid=21995386}}</ref><ref>{{Cite journal|last=L|first=Malcovati|last2=M|first2=Karimi|last3=E|first3=Papaemmanuil|last4=I|first4=Ambaglio|last5=M|first5=Jädersten|last6=M|first6=Jansson|last7=C|first7=Elena|last8=A|first8=Gallì|last9=G|first9=Walldin|date=2015|title=SF3B1 Mutation Identifies a Distinct Subset of Myelodysplastic Syndrome With Ring Sideroblasts|url=https://pubmed.ncbi.nlm.nih.gov/25957392/|language=en|doi=10.1182/blood-2015-03-633537|pmc=PMC4528082|pmid=25957392}}</ref>.

{| class="wikitable sortable"
|-
!Gene!!Mutation!!Oncogene/Tumor Suppressor/Other!!Presumed Mechanism (LOF/GOF/Other; Driver/Passenger)!!Prevalence (COSMIC/TCGA/Other)
|-
|EXAMPLE TP53||EXAMPLE R273H||EXAMPLE Tumor Suppressor||EXAMPLE LOF||EXAMPLE 20%
|}

===Other Mutations===
{| class="wikitable sortable"
|-
!Type!!Gene/Region/Other
|-
|Concomitant Mutations||EXAMPLE IDH1 R123H
|-
|Secondary Mutations||EXAMPLE Trisomy 7
|-
|Mutually Exclusive||EXAMPLE EGFR Amplification
|}

==Epigenomics (Methylation)==

Genes involved in epigenetic regulation are frequently mutated in MDS such as TET2, DNMT3A, IDH1, IDH2, AXSL1, and EZH2 <ref>{{Cite journal|last=M|first=Heuser|last2=H|first2=Yun|last3=F|first3=Thol|date=2018|title=Epigenetics in Myelodysplastic Syndromes|url=https://pubmed.ncbi.nlm.nih.gov/28778402/|language=en|pmid=28778402}}</ref> . These genes play a role in DNA methylation and chromatin modification as well as regulating gene expression. In low risk MDS such as MDS-RS, mutations in these genes can coexist with SF3B1 mutation and seem to be associated with MDS-RS-MLD <ref>{{Cite journal|last=L|first=Malcovati|last2=M|first2=Karimi|last3=E|first3=Papaemmanuil|last4=I|first4=Ambaglio|last5=M|first5=Jädersten|last6=M|first6=Jansson|last7=C|first7=Elena|last8=A|first8=Gallì|last9=G|first9=Walldin|date=2015|title=SF3B1 Mutation Identifies a Distinct Subset of Myelodysplastic Syndrome With Ring Sideroblasts|url=https://pubmed.ncbi.nlm.nih.gov/25957392/|language=en|doi=10.1182/blood-2015-03-633537|pmc=PMC4528082|pmid=25957392}}</ref>.

==Genes and Main Pathways Involved==

''SF3B1'' gene encodes a protein that is part of the U2 snRNP protein complex which functions as splicing machinery to regulate pre-mRNA maturation. Studies have shown that mutated ''SF3B1'' tends to utilize alternative branch point sequence to direct the U2 snRNP to an altered 3' splice site and therefore produces aberrantly spliced mRNAs which are frequently subjected to nonsense-mediated decay <ref>{{Cite journal|last=Rb|first=Darman|last2=M|first2=Seiler|last3=Aa|first3=Agrawal|last4=Kh|first4=Lim|last5=S|first5=Peng|last6=D|first6=Aird|last7=Sl|first7=Bailey|last8=Eb|first8=Bhavsar|last9=B|first9=Chan|date=2015|title=Cancer-Associated SF3B1 Hotspot Mutations Induce Cryptic 3' Splice Site Selection Through Use of a Different Branch Point|url=https://pubmed.ncbi.nlm.nih.gov/26565915/|language=en|pmid=26565915}}</ref> . The mechanisms of how spliceosome defect leads to accumulation of BM RS are still unclear. In patients with ''SF3B1'' mutations, the transcriptome profile shows that genes involved in mitochondrial ribosome and electron transport chain were significantly down-regulated <ref>{{Cite journal|last=E|first=Papaemmanuil|last2=M|first2=Cazzola|last3=J|first3=Boultwood|last4=L|first4=Malcovati|last5=P|first5=Vyas|last6=D|first6=Bowen|last7=A|first7=Pellagatti|last8=Js|first8=Wainscoat|last9=E|first9=Hellstrom-Lindberg|date=2011|title=Somatic SF3B1 Mutation in Myelodysplasia With Ring Sideroblasts|url=https://pubmed.ncbi.nlm.nih.gov/21995386/|language=en|doi=10.1056/NEJMoa1103283|pmc=PMC3322589|pmid=21995386}}</ref> . ''ABCB7,'' a transporter gene that mediate heme homeostasis, previously known to cause congenital sideroblastic anemia, was found to be down-regulated by aberrant splicing in SF3B1 mutated erythroid blasts <ref>{{Cite journal|last=M|first=Nikpour|last2=C|first2=Scharenberg|last3=A|first3=Liu|last4=S|first4=Conte|last5=M|first5=Karimi|last6=T|first6=Mortera-Blanco|last7=V|first7=Giai|last8=M|first8=Fernandez-Mercado|last9=E|first9=Papaemmanuil|date=2013|title=The Transporter ABCB7 Is a Mediator of the Phenotype of Acquired Refractory Anemia With Ring Sideroblasts|url=https://pubmed.ncbi.nlm.nih.gov/23070040/|language=en|doi=10.1038/leu.2012.298|pmc=PMC3794445|pmid=23070040}}</ref> . A recent study showed a variant transcript of erythroferrone was elevated in MDS patients with an ''SF3B1'' mutations and is responsible for hepcidin suppression and iron overload <ref>{{Cite journal|last=S|first=Bondu|last2=As|first2=Alary|last3=C|first3=Lefèvre|last4=A|first4=Houy|last5=G|first5=Jung|last6=T|first6=Lefebvre|last7=D|first7=Rombaut|last8=I|first8=Boussaid|last9=A|first9=Bousta|date=2019|title=A Variant Erythroferrone Disrupts Iron Homeostasis in SF3B1-mutated Myelodysplastic Syndrome|url=https://pubmed.ncbi.nlm.nih.gov/31292266/|language=en|pmid=31292266}}</ref> .

In addition to spliceosome pathway, DNA methylators, chromatin modifiers and transcription factors are among the most frequently mutated categories in MDS-RS. The prognostic and therapeutic values remain to be elucidated.

==Diagnostic Testing Methods==

*Morphology

*Blood test
*BM aspirate
*Iron staining: Prussian blue (Peals reaction)
*Histomorphology
*Cytogenetics/FISH studies
*Molecular analysis: Sanger sequencing, Next Generation Sequencing

==Clinical Significance (Diagnosis, Prognosis and Therapeutic Implications)==

The diagnosis of MDS-RS-MLD needs to meet MDS-RS diagnosis criteria and in addition include:

*≥ 10% dysplasisa in two or more myeloid lineages (MDS-RS-MLD)

*Exclusions include: non-clonal dysplasia, therapy-related myeloid neoplasm, isolated del(5q), and secondary causes of RS

Prognosis:

*IPSS (international prognostic scoring system) <ref>{{Cite journal|last=P|first=Greenberg|last2=C|first2=Cox|last3=Mm|first3=LeBeau|last4=P|first4=Fenaux|last5=P|first5=Morel|last6=G|first6=Sanz|last7=M|first7=Sanz|last8=T|first8=Vallespi|last9=T|first9=Hamblin|date=1997|title=International Scoring System for Evaluating Prognosis in Myelodysplastic Syndromes|url=https://pubmed.ncbi.nlm.nih.gov/9058730/|language=en|pmid=9058730}}</ref> , R-IPSS (revised IPSS) and WPSS (WHO classification based prognostic scoring system) <ref>{{Cite journal|last=L|first=Malcovati|last2=U|first2=Germing|last3=A|first3=Kuendgen|last4=Mg|first4=Della Porta|last5=C|first5=Pascutto|last6=R|first6=Invernizzi|last7=A|first7=Giagounidis|last8=B|first8=Hildebrandt|last9=P|first9=Bernasconi|date=2007|title=Time-dependent Prognostic Scoring System for Predicting Survival and Leukemic Evolution in Myelodysplastic Syndromes|url=https://pubmed.ncbi.nlm.nih.gov/17687155/|language=en|pmid=17687155}}</ref> are widely used scoring systems to evaluate MDS prognosis.

*The median survival of MDS-RS-MLD is 28 months [WHO].

*8% in MDS-RS-MLD[WHO] cases progress to [[AML|acute myeloid leukemia]].

*SF3B1 mutation is thought to have favorable prognosis when no other adverse factors in present.

*Mutations in the TP53, EZH2, ETV6, RUNX1, and ASXL1 are reported to be associated with shorter survival <ref>{{Cite journal|last=R|first=Bejar|last2=K|first2=Stevenson|last3=O|first3=Abdel-Wahab|last4=N|first4=Galili|last5=B|first5=Nilsson|last6=G|first6=Garcia-Manero|last7=H|first7=Kantarjian|last8=A|first8=Raza|last9=Rl|first9=Levine|date=2011|title=Clinical Effect of Point Mutations in Myelodysplastic Syndromes|url=https://pubmed.ncbi.nlm.nih.gov/21714648/|language=en|doi=10.1056/NEJMoa1013343|pmc=PMC3159042|pmid=21714648}}</ref> . SF3B1<sup>mutant</sup>/ASXL1<sup>wildtype</sup> genotype is of the most favorable prognosis whereas ASXL1 independently confers adverse prognosis <ref>{{Cite journal|last=Aa|first=Mangaonkar|last2=Tl|first2=Lasho|last3=Cm|first3=Finke|last4=N|first4=Gangat|last5=A|first5=Al-Kali|last6=Ma|first6=Elliott|last7=Kh|first7=Begna|last8=H|first8=Alkhateeb|last9=Ap|first9=Wolanskyj-Spinner|date=2018|title=Prognostic Interaction Between Bone Marrow Morphology and SF3B1 and ASXL1 Mutations in Myelodysplastic Syndromes With Ring Sideroblasts|url=https://pubmed.ncbi.nlm.nih.gov/29434284/|language=en|doi=10.1038/s41408-018-0051-1|pmc=PMC5809387|pmid=29434284}}</ref> .

Therapeutic Implications:

*Allogeeic hematopoietic stem cell transplantation (HSCT) is the only curative treatment for patients with MDS.

*Treatment of anemia: recombinant human erythropoietin, darbepoetin

*Immunomodulatory agents: Lenalidomide, TGF-β inhibitors such as Sotatercept and Luspatercept.

*Iron chelation therapy if iron overload.Hypomethylating agents are under investigation.

·

==Familial Forms==

Put your text here

==Other Information==

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==Links==

Put your links here (use "Link" icon at top of page)

==References==
(use "Cite" icon at top of page)
<references />
===EXAMPLE Book===

#Arber DA, et al., (2017). Acute myeloid leukaemia with recurrent genetic abnormalities, in World Health Organization Classification of Tumours of Haematopoietic and Lymphoid Tissues, Revised 4th edition. Swerdlow SH, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J, Arber DA, Hasserjian RP, Le Beau MM, Orazi A, and Siebert R, Editors. IARC Press: Lyon, France, p129-171.

==Notes==
<nowiki>*</nowiki>Primary authors will typically be those that initially create and complete the content of a page. If a subsequent user modifies the content and feels the effort put forth is of high enough significance to warrant listing in the authorship section, please contact the CCGA coordinators (contact information provided on the homepage). Additional global feedback or concerns are also welcome.

HAEM4:Myelodysplastic Syndrome with Ring Sideroblasts and Multilineage Dysplasia - Revision history

Bailey.Glen at 21:24, 4 December 2023

Bailey.Glen at 18:42, 3 November 2023

Bailey.Glen: Created page with " ==Primary Author(s)*== Xiaolin Hu, Ph.D., Teresa Smolarek, Ph.D, FACMG __TOC__ ==Cancer Category/Type== Myelodysplastic Syndrome (MDS) ==Cancer Sub-Classification / Subt..."

Bailey.Glen: Created page with " ==Primary Author(s)*== Xiaolin Hu, Ph.D., Teresa Smolarek, Ph.D, FACMG TOC ==Cancer Category/Type== Myelodysplastic Syndrome (MDS) ==Cancer Sub-Classification / Subt..."